The CURE: VA/UCLA Gastroenteric Biology Center is composed of a cohesive group of physicians and basic scientists with strong independent grant- supported research program in gut biology, with special emphasis upon mucosal physiology and disease. CURE first received NIDDK funding in 1974 as a Center to study peptic ulcer disease and became a Digestive Disease Core Center in 1989. The research emphasis of the center is acquisition of new knowledge about cellular processes and physiological control of the gut and translation of this knowledge into development of therapy for patients with gastrointestinal diseases. CURE initially established its reputation for work in clinical peptic ulcer disease, physiological regulation of acid secretion, and parietal cell mechanisms for secreting acid. More recently, demonstration that Helicobacter pylori is an essential factor in pathogenesis of ordinary peptic ulcer disease has brought new aspects of mucosal cell biology into the forefront as the next frontier of research that CURE will follow in its third decade. The interests and activities of Center members have evolved along with science in this area and now include several facets of gastrointestinal regulatory biology including gastrointestinal regulatory peptides, brain-gut interactions, and membrane transport as well as diseases related to these areas. In addition to the parietal cell, other new mucosal cell models have been developed for studies by Center investigators. Functional bowel disease, inflammatory bowel disease, and other disorders of intestinal mucosal function have joined peptic diseases as clinical applications of basic science. The five scientific cores outlined in this proposal provide ready access to technology and to clinical and biological materials that are essential to the programs of Center members. These cores provide custom antibody production, sophisticated peptide chemistry techniques, access to modern cellular imaging to study membrane proteins and their functions, animal models for studying physiology and pathophysiology, and access to a broad range of techniques and patients for clinical studies. An administrative core provides a wide range of administrative support for members and for Center activities including a dynamic enrichment program. The pilot and feasibility program has provided a successful mechanism for aiding development of new research programs by young investigators, and recipients usually have obtained independent funding. The Center provides an optimal environment for cooperation and collaboration among its investigators, who have had a major impact on mucosal biology and on peptic ulcer disease over the past two decades and promise to have an even larger impact upon expanded research areas with continued support from the Center.

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Center Core Grants (P30)
Project #
5P30DK041301-10
Application #
2838108
Study Section
Diabetes, Endocrinology and Metabolic Diseases B Subcommittee (DDK)
Program Officer
Podskalny, Judith M,
Project Start
1990-01-15
Project End
1999-11-30
Budget Start
1999-03-15
Budget End
1999-11-30
Support Year
10
Fiscal Year
1999
Total Cost
Indirect Cost
Name
University of California Los Angeles
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
119132785
City
Los Angeles
State
CA
Country
United States
Zip Code
90095
Henström, Maria; Diekmann, Lena; Bonfiglio, Ferdinando et al. (2018) Functional variants in the sucrase-isomaltase gene associate with increased risk of irritable bowel syndrome. Gut 67:263-270
Soroosh, Artin; Koutsioumpa, Marina; Pothoulakis, Charalabos et al. (2018) Functional role and therapeutic targeting of microRNAs in inflammatory bowel disease. Am J Physiol Gastrointest Liver Physiol 314:G256-G262
Aschemeyer, Sharraya; Qiao, Bo; Stefanova, Deborah et al. (2018) Structure-function analysis of ferroportin defines the binding site and an alternative mechanism of action of hepcidin. Blood 131:899-910
Kaji, I; Akiba, Y; Furuyama, T et al. (2018) Free fatty acid receptor 3 activation suppresses neurogenic motility in rat proximal colon. Neurogastroenterol Motil 30:
Kim, Paul H; Luu, Jennings; Heizer, Patrick et al. (2018) Disrupting the LINC complex in smooth muscle cells reduces aortic disease in a mouse model of Hutchinson-Gilford progeria syndrome. Sci Transl Med 10:
Dong, Tien S; Aby, Elizabeth S; Benhammou, Jihane N et al. (2018) Metabolic syndrome does not affect sustained virologic response of direct-acting antivirals while hepatitis C clearance improves hemoglobin A1c. World J Hepatol 10:612-621
Videlock, Elizabeth J; Mahurkar-Joshi, Swapna; Hoffman, Jill M et al. (2018) Sigmoid colon mucosal gene expression supports alterations of neuronal signaling in irritable bowel syndrome with constipation. Am J Physiol Gastrointest Liver Physiol 315:G140-G157
Chen, Natalie Y; Kim, Paul; Weston, Thomas A et al. (2018) Fibroblasts lacking nuclear lamins do not have nuclear blebs or protrusions but nevertheless have frequent nuclear membrane ruptures. Proc Natl Acad Sci U S A 115:10100-10105
Larauche, Muriel; Moussaoui, Nabila; Biraud, Mandy et al. (2018) Brain corticotropin-releasing factor signaling: Involvement in acute stress-induced visceral analgesia in male rats. Neurogastroenterol Motil :e13489
Zhou, Haoming; Wang, Han; Ni, Ming et al. (2018) Glycogen synthase kinase 3? promotes liver innate immune activation by restraining AMP-activated protein kinase activation. J Hepatol 69:99-109

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